RhoBTB3, an atypical Rho GTPase family member, is involved in multiple cellular functions. It binds and hydrolyzes ATP, participating in diverse pathways such as endosome to Golgi transport, autophagy regulation, and cell cycle control. Its functions are crucial for maintaining cellular homeostasis and are relevant to various disease processes [4,2,6].

In breast cancer, decreasing RhoBTB3 expression leads to reduced proliferative and invasive properties of cancer cells, potentially through repressing Col1a1 expression, suggesting its role in tumor progression [1]. In autophagy, RhoBTB3 deficiency induces autophagy, while overexpression inhibits it by mediating the ubiquitination and degradation of AMBRA1 [2]. In renal carcinomas, its deficiency significantly elevates the Warburg effect and accelerates xenograft growth, as it promotes proteasomal degradation of HIFα [3]. In non-M3 acute myeloid leukemia, high RhoBTB3 expression predicts favorable chemotherapy outcomes [5].

In conclusion, RhoBTB3 plays essential roles in multiple biological processes and disease conditions. Research using gene knockout models, like in mice, has revealed its significance in cancer progression, autophagy, and treatment response in leukemia. Understanding RhoBTB3's functions provides potential therapeutic targets for related diseases.